Lnc-RNA UCA1 Promotes TGF-β-Mediated Epithelial-Mesenchymal Transition via Inhibiting miR-204 in Gastric Cancer Cells

Abstract

Introduction Cancer is a genetic modification disease. Since genetic aberrations of gastric cancer are heterogeneous, we assume non-coding RNAs play major roles on gastric cancer phenotypes. Long non-coding RNA (lncRNA) urothelial cancer associated 1 (UCA1) is related with poor prognosis in different cancer types, however, how it works in gastric cancer is unknown. Methods Two gastric cancer cell lines are chosen, MNK45 and SGC-7901. Transforming growth factor-β (TGF-β) is used to promote epithelial-mesenchymal transition (EMT) by using cancer cell invasion assay. The transmembrane cell quantities are counted and ZEB1, slug, vimentine and E-Cadherin gene expression levels are measured by quantitative PCR assay. siRNA of UCA1 and miR-204 are used to confirm cross-talk among TGF-β, UCA1 and miR-204. Results TGF-β significantly increases gastric cancer cell transmembrane ability and expression levels of four EMT related genes. These increases can be counteracted by using siRNA of UCA1, suggesting that UCA1 is up-stream factor of TGF-β signaling pathways and positively regulates it. miRNA-204 alone can inhibit ZEB1 gene expression, however, this inhibition can be demolished by UCA1, suggesting that UCA1 sponges miR-204 to prevent its function from inhibiting ZEB1. Conclusions miR-204 could be used as an indicator of prognosis of gastric cancer. The higher miR-204 expression levels, the less possibility to develop EMT. Meanwhile, UCA1 inhibitors can be considered as potential genetic medical drugs.